In vivo, the RLC phosphorylation was shown to be a significant modulatory mechanism of myosin activation and muscle contraction, and a severely decreased level of RLC phosphorylation was observed in the hearts of HCM and/or heart failure patients (Van Der Velden et al., 2003a,b,c) and in the animal models of HCM (Abraham et al., 2009; Muthu et al., 2010, 2012; Yuan et al., 2015). This evidence concerns the gene MYH14 and heart failure.